A5032005014- Neuroscience and Neuropharmacology Research
- Neurotransmitter Receptor Influence on Behavior
- Neuroinflammation and Neurodegeneration Mechanisms
- Pain Mechanisms and Treatments
- Stress Responses and Cortisol
- Barrier Structure and Function Studies
- Neuropeptides and Animal Physiology
- Cannabis and Cannabinoid Research
- Parkinson's Disease Mechanisms and Treatments
- Receptor Mechanisms and Signaling
- Neurological Disease Mechanisms and Treatments
- Heart Rate Variability and Autonomic Control
- Traumatic Brain Injury and Neurovascular Disturbances
- Memory and Neural Mechanisms
- Immune cells in cancer
- Cellular transport and secretion
- Immune Response and Inflammation
- Peroxisome Proliferator-Activated Receptors
- Ion channel regulation and function
- Carcinogens and Genotoxicity Assessment
- Pharmacogenetics and Drug Metabolism
- Animal Ecology and Behavior Studies
- Environmental Toxicology and Ecotoxicology
- Ferroptosis and cancer prognosis
- Neurological disorders and treatments
MIND Research Institute
2013-2025
Cornell University
2011-2025
University of Notre Dame
2025
Weill Cornell Medicine
2016-2022
Washington State University Vancouver
2003-2005
Washington State University
2004
Ontario Neurotrauma Foundation
1997
Louisiana State University
1997
University Medical Center New Orleans
1997
Max Planck Institute for Biophysical Chemistry
1979
Hypertension is a leading risk factor for dementia, but the mechanisms underlying its damaging effects on brain are poorly understood. Due to lack of energy reserves, relies continuous delivery blood flow active regions in accordance with their dynamic metabolic needs. disrupts these vital regulatory mechanisms, neuronal dysfunction and damage cognitive impairment. Elucidating cellular bases impairments essential developing new therapies. Perivascular macrophages (PVMs) represent distinct...
Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery blood flow the brain. also alters blood-brain barrier (BBB), critical component brain health. Although endothelial cells are ultimately responsible for BBB, development maintenance properties depend on interaction with other vascular-associated cells. However, it remains unclear if BBB disruption in hypertension requires cooperative Perivascular macrophages (PVM), innate immune closely...
Background and Purpose- Commensal gut bacteria have a profound impact on stroke pathophysiology. Here, we investigated whether modification of the microbiota influences acute long-term outcome in mice subjected to stroke. Methods- C57BL/6 male received cocktail antibiotics or single antibiotic. After 4 weeks, fecal bacterial density 16S rRNA gene was quantitated by qPCR, phylogenetic classification obtained sequencing. Infarct volume hemispheric loss were measured 3 days 5 weeks after middle...
Abstract Considerable evidence supports the release of pathogenic aggregates neuronal protein α-Synuclein (αSyn) into extracellular space. While this is proposed to instigate neuron-to-neuron transmission and spread αSyn pathology in synucleinopathies including Parkinson’s disease, molecular-cellular mechanism(s) remain unclear. To study this, we generated a new mouse model specifically immunoisolate lysosomes, established long-term culture where are produced within neurons without addition...
Loss-of-function mutations of progranulin (PGRN) have been linked to frontotemporal dementia, but little is known about the effects PGRN deficiency on brain in health and disease. has implicated neurovascular development, inflammation, Wnt signaling, a pathway involved formation blood–brain barrier (BBB). Because BBB alterations inflammation contribute ischemic injury, we examined role damage produced by ischemia-reperfusion. +/− −/− mice underwent middle cerebral artery occlusion (MCAO)...
Exposure to low-dose lipopolysaccharide (LPS) before cerebral ischemia is neuroprotective in stroke models, a phenomenon termed preconditioning (PC). Although it well established that LPS-PC induces central and peripheral immune responses, the cellular mechanisms modulating ischemic injury remain unclear. Here, we investigated role of cells brain protection afforded by PC tested whether monocytes may be reprogrammed ex vivo LPS exposure, thus inflammatory after male mice. We found systemic...
Lipid second messengers such as arachidonic acid and its metabolites diacylglycerols (DAGs) are affected in brain injury. Therefore, changes the pool size fatty composition of free acids (FFAs) DAGs were analyzed different rat areas 4 35 days after traumatic Cortical impact injury low-grade severity was applied right frontal somatosensory cortex. Four injury, FFAs increased by three- twofold, respectively, injured cortex to a lesser extent contralateral compared with sham-operated animals....
Opiate addiction is characterized by progressive increases in drug intake over time suggesting maladaptive changes motivational and reward systems. These behaviors are mediated dopaminergic neurons originating from the ventral tegmental area (VTA), long-term of these attributed to increased postsynaptic glutamatergic activation. Indeed, chronic morphine administration known increase AMPA receptor glutamate 1 (GluR1) subunit VTA. However, there no ultrastructural evidence that affects...
Neurotransmitter release occurs through exocytosis of synaptic vesicles. α-Synuclein's function and dysfunction in Parkinson's disease other synucleinopathies is thought to be tightly linked vesicle binding. Age the biggest risk factor for synucleinopathy, ~15% proteins have been central nervous system diseases. Yet, age- disease-induced changes vesicles remain unexplored. Via systematic analysis at ultrastructural, protein, lipid levels, we reveal specific populations, proteins, lipids over...
Cannabinoid-type 1 (CB1) receptors are implicated in μ-opioid receptor (μ-OR)-dependent reward ascribed partially to mesolimbic dopamine release the nucleus accumbens (Acb) shell. Thus, CB1 gene deletion may preferentially alter availability of μ-ORs and/or innervation this brain region, which is functionally distinct from motor-associated Acb core. To test hypothesis, we examined electron microscopic immunolabeling μ-OR and dopamine-synthesizing enzyme, tyrosine hydroxylase (TH) shell, core...
The nucleus accumbens (Acb) shell and caudate-putamen (CPu) are respectively implicated in the motivational motor effects of dopamine, which mediated part through dopamine D₂-like receptors (D₂Rs) modulated by activation cannabinoid-1 receptor (CB₁R). D(₂/D3) agonist, quinpirole elicits internalization D₂Rs isolated cells; however, dendritic axonal targeting may be highly influenced circuit-dependent changes vivo potentially endogenous CB₁R activation.We sought to determine whether alters...